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Role of adhesive proteins in platelet tumor interaction in vitro and metastasis formation in vivo
S Karpatkin1, E Pearlstein, C Ambrogio
1Department of Medicine, New York University Medical Center, New York 10016.
The Journal of Clinical Investigation
|April 1, 1988
Summary
Platelets promote tumor metastasis through adhesion to cancer cells via fibronectin and von Willebrand factor. Blocking these interactions significantly reduces tumor spread in vivo, highlighting a novel therapeutic target.
Area of Science:
- Oncology
- Hematology
- Cell Biology
Background:
- Platelet-tumor cell interactions are implicated in cancer metastasis.
- Specific platelet surface receptors and adhesive proteins mediate these interactions.
Purpose of the Study:
- To investigate the role of platelet-adhesive proteins, fibronectin and von Willebrand factor, in tumor cell adhesion and metastasis.
- To determine the in vitro and in vivo efficacy of blocking these interactions.
Main Methods:
- In vitro co-culture assays using colon carcinoma cells and platelets.
- In vivo studies using mouse models of pulmonary metastasis.
- Inhibition studies using monoclonal antibodies (10E5, 3B2, 6D1) and peptide inhibitors (RGDS).
- Assessment of anti-fibronectin and anti-von Willebrand factor antibodies.
Main Results:
- Monoclonal antibody 10E5 and RGDS peptide significantly inhibited tumor cell binding to platelets in vitro.
- Anti-fibronectin and anti-von Willebrand factor antibodies also reduced tumor cell adhesion.
- In vivo, anti-von Willebrand factor antibody decreased pulmonary metastases for multiple tumor types.
- Platelet infusion reconstituted metastasis, and this could be blocked by antibody 10E5.
Conclusions:
- Platelet adhesion to tumor cells, mediated by fibronectin and von Willebrand factor, contributes to cancer metastasis.
- Targeting these specific platelet-tumor cell interactions offers a potential strategy for inhibiting metastasis.